Anabolic steroids (AS) derived from testosterone have both anabolic (muscle and strength enhancing) and a n d r o g e n i c (primary and s e c o n d a r y sexual) effects. Efforts to limit the androgenic while enhancing the anabolic effects have not been successful. Alterations to the structure of testosterone, so as to improve the pharmacokinetics of AS, have resulted in drugs, which are orally active, have a longer plasma half life and may be administered as depot injections. Therapeutic doses of AS produce statistically significant effects on strength and athletic performance in well-controlled scientific and clinical trials. At low, therapeutic doses, diet and an intensive training regime are equally important in producing a statistically significant increase in strength. Higher doses 6-7000mg per week are regularly administered in sport and produce the greatest increases in muscle strength erythropoiesis and lean body mass. Patterns of steroid abuse can be complex, reflecting a desire to minimise side effects, and avoid detection. AS side effects are of many types. AS increase salt and water retention leading to an expansion of the blood volume, but effects of steroids on blood pressure are equivocal and most cardiovascular side effects appear to be reversible.Abuse of AS causes an increase in blood triglyceride and cholesterol levels and this is associated with a decline in High Density Lipoproteins (HDLs) and an increase in the Low Density (LDL) type. Though these effects are reversible they are associated with an increased risk of both acute and c h r o n i c c a r d i o v a s c u l a r p a t h o l o g y . The m o s t serious irreversible anabolic steroid side effects are associated with carcinomas -mainly of the liver, prostate and kidney. Hepatic carcinomas are strongly associated with abuse of the orally active 17alpha methyl substituted steroids, which also produce a reversible jaundice. In males, anabolic steroid abuse causes suppression of LH and FSH release leading to inhibition of testosterone production often accompanied by testicular atrophy, and azoospermia. High, chronic doses of the drugs may also cause moderate to severe feminising effects in the form of gynaecomastia. Male secondary sexual characteristics are a side effect of AS abuse in women. Increased insulin resistance and elevated fasting blood glucose levels are the commonest non-gonadal endocrine side effects of AS.AS abuse leads to contradictory, complex, behavioural, and psychiatric changes. Increased frequency of mental illness, in anabolic steroid abusers including paranoid schizophrenia, mania and d e p r e s s i o n has been r e p o r t e d . P h y s i c a l and psychological dependency occur amongst some anabolic steroid abusers and severe psychiatric disorders can appear upon withdrawal, leading in a few cases to criminality and even suicide. We need more studies on the long-term effects of AS. The implications of the past 50 years of AS abuse will be discussed in the review.

Anabolic steroids (AS) derived from testosterone have both anabolic (muscle and strength enhancing) and a n d r o g e n i c (primary and s e c o n d a r y sexual) effects. Efforts to limit the androgenic while enhancing the anabolic effects have not been successful. Alterations to the structure of testosterone, so as to improve the pharmacokinetics of AS, have resulted in drugs, which are orally active, have a longer plasma half life and may be administered as depot injections. Therapeutic doses of AS produce statistically significant effects on strength and athletic performance in well-controlled scientific and clinical trials. At low, therapeutic doses, diet and an intensive training regime are equally important in producing a statistically significant increase in strength. Higher doses 6-7000mg per week are regularly administered in sport and produce the greatest increases in muscle strength erythropoiesis and lean body mass. Patterns of steroid abuse can be complex, reflecting a desire to minimise side effects, and avoid detection. AS side effects are of many types. AS increase salt and water retention leading to an expansion of the blood volume, but effects of steroids on blood pressure are equivocal and most cardiovascular side effects appear to be reversible.Abuse of AS causes an increase in blood triglyceride and cholesterol levels and this is associated with a decline in High Density Lipoproteins (HDLs) and an increase in the Low Density (LDL) type. Though these effects are reversible they are associated with an increased risk of both acute and c h r o n i c c a r d i o v a s c u l a r p a t h o l o g y . The m o s t serious irreversible anabolic steroid side effects are associated with carcinomas -mainly of the liver, prostate and kidney. Hepatic carcinomas are strongly associated with abuse of the orally active 17alpha methyl substituted steroids, which also produce a reversible jaundice. In males, anabolic steroid abuse causes suppression of LH and FSH release leading to inhibition of testosterone production often accompanied by testicular atrophy, and azoospermia. High, chronic doses of the drugs may also cause moderate to severe feminising effects in the form of gynaecomastia. Male secondary sexual characteristics are a side effect of AS abuse in women. Increased insulin resistance and elevated fasting blood glucose levels are the commonest non-gonadal endocrine side effects of AS.AS abuse leads to contradictory, complex, behavioural, and psychiatric changes. Increased frequency of mental illness, in anabolic steroid abusers including paranoid schizophrenia, mania and d e p r e s s i o n has been r e p o r t e d . P h y s i c a l and psychological dependency occur amongst some anabolic steroid abusers and severe psychiatric disorders can appear upon withdrawal, leading in a few cases to criminality and even suicide. We need more studies on the long-term effects of AS. The implications of the past 50 years of AS abuse will be discussed in the review.

unselected thyrotoxic patients were prescribed 200 MBq radioactive iodine ( 131 I). None of these patients received a thionamide such as carbimazole or propylthiouracil within two weeks of treatment or subsequently. Symptom relief was achieved using blockers alone. Remission at one year was achieved in 84% of these patients and of these 62% were hypothyroid and taking thyroxine. Within this time, re-treatment of those who remained thyrotoxic achieved an overall success rate at one year of 95%. The outcome of 164 similar patients prescribed 250-400 MBq 131 I between 1996 and 2001 gave comparable results. The failure rate after a single 200 MBq 131 I dose was significantly lower than that previously published where 185 MBq 131 I and thionamides had been used. Our low-dose strategy has the potential for halving the radiation exposure to the patient and the environment, when compared with the ablative strategies in common use. KEY WORDS: radioiodine, thionamide, thyrotoxicosis IntroductionRadioactive iodine ( 131 I) therapy has been used for over 60 years to treat patients with thyrotoxicosis, 1 and in some departments it accounts for 79% of referrals for definitive treatment of adults with this condition. 2 Guidelines formulated by the Royal College of Physicians in 1995 recommended that doses of 300-800 MBq 131 I should be used, and that thionamide therapy, such as carbimazole or propylthiouracil, should be given to most patients unless the thyrotoxicosis was mild. 3 Lower doses of 131 I were regarded as inadequate, but the outcome in those studies had been compromised by the concomitant use of thionamides, 4-7 which have been shown to reduce the effectiveness of 131 I by up to 44%. 8 Doses of 520-555 MBq of 131 I will achieve remission rates between 91 and 94% at one year, 9-11 but a clear statement regarding an outcome target is lacking.It is, however, important to minimise the potential therapeutic hazard of exposing patients and the environment to non-essential radiation. In the light of these considerations, we examined the efficacy of a fixed dose of 200 MBq 131 I compared with larger doses, prescribed in our department over the last five years, for thyrotoxic patients whose symptoms were modified by beta-adrenergic blocking drugs alone, and compared our results with the published data. Patients and methodsFrom 1996 to June 2001 all thyrotoxic patients referred to the Endocrine Department, and who subsequently received 131 I treatment, were entered on our thyroid register. Patients presenting with subacute thyroiditis and those in whom the free thyroxine (FT4) was 22 pmol/l or the thyroidstimulating hormone (TSH) was detectable, were not considered suitable candidates for 131 I treatment. All patients had been given an information package and at a subsequent visit those considered suitable were able to choose from three options: treatment with a thionamide, surgery or 131 I.The dose of 131 I prescribed was either 200 MBq or 250-400 MBq. This was given as a 131 I capsule. The majority of the patients for who...

Azathioprine is an established immunosuppressive agent in the treatment of myasthenia gravis. In rare cases, complications such as hypersensitivity reactions including fever may occur. A 73-year-old patient with the first manifestation of myasthenia gravis was immunosuppressed with azathioprine and prednisolone in addition to pyridostigmine treatment and discharged from hospital without symptoms. Ten days after onset of azathioprine therapy, he developed fever and a myasthenic crisis requiring artificial ventilation. Azathioprine was discontinued. Microbiological and radiological examinations revealed no signs of infection. After clinical improvement azathioprine was re-started, and following a single dose the patient again presented with fever and tachycardia. Azathioprine was discontinued, and all symptoms abated within a day. These symptoms were most probably caused by an azathioprine-induced hypersensitivity reaction. Life-threatening myasthenic crises may occur if such a hypersensitivity reaction remains unrecognized in patients with myasthenia gravis.